SummaryDefence against pathogens in Arabidopsis is orchestrated by at least three signalling molecules: salicylic acid (SA), jasmonic acid (JA) and ethylene (ET). The hrl1 (hypersensitive response-like lesions 1) mutant of Arabidopsis is characterized by spontaneous necrotic lesions, accumulation of reactive oxygen species, constitutive expression of SA-and ET/JA-responsive defence genes, and enhanced resistance to virulent bacterial and oomycete pathogens. Epistasis analyses of hrl1 with npr1, etr1, coi1 and SAdepleted nahG plants revealed novel interactions between SA and ET/JA signalling pathways in regulating defence gene expression and cell death. RNA gel-blot analysis of RNA isolated separately from the lesion + and the lesion ± leaves of double mutants of hrl1 revealed different signalling requirements for the expression of defence genes in these tissues. Expression of the ET/JA-responsive PDF1.2 gene was markedly reduced in hrl1 npr1 and in SA-depleted hrl1 nahG plants. In hrl1 nahG plants, expression of PDF1.2 was regulated by benzathiadiazole in a concentration-dependent manner: induced at low concentration and suppressed at high concentration. The hrl1 etr1 plants lacked systemic PR-1 expression, and exhibited compromised resistance to virulent Pseudomonas syringae and Peronospora parasitica. Inhibiting JA responses in hrl1 coi1 plants lead to exaggerated cell death and severe stunting of plants. Finally, the hrl1 mutation lead to elevated expression of AtrbohD, which encodes a major subunit of the NADPH oxidase complex. Our results indicate that defence gene expression and resistance against pathogens in hrl1 is regulated synergistically by SA and ET/JA defence pathways.

SummaryWe describe the characterization of a novel gain-of-function Arabidopsis mutant, dll1 (disease-like lesions1), which spontaneously develops lesions mimicking bacterial speck disease and constitutively expresses biochemical and molecular markers associated with pathogen infection. Despite the constitutive expression of defense-related responses, dll1 is unable to suppress the growth of virulent pathogens. However, dll1 elicits normal hypersensitive response in response to avirulent pathogens, thus indicating that dll1 is not defective in the induction of normal resistance responses. The lesion + leaves of dll1 support the growth of hrcC mutant of Pseudomonas syringae, which is defective in the transfer of virulence factors into the plant cells, and therefore non-pathogenic to wild-type Col-0 plants. This suggests that dll1 intrinsically expresses many of the cellular processes that are required for pathogen growth during disease. Epistasis analyses reveal that salicylic acid and NPR1 are required for lesion formation, while ethylene modulates lesion development in dll1, suggesting that signi®cant overlap exist between the signalling pathways leading to resistance-and disease-associated cell death. Our results suggest that host cell death during compatible interactions, at least in part, is genetically controlled by the plant and DLL1 may positively regulate this process.

The hypersensitive response (HR) displayed by resistant plants against invading pathogens is a prominent feature of plant-pathogen interactions. The Arabidopsis hypersensitive response like lesions1 (hrl1) mutant is characterized by heightened defense responses that make it more resistant to virulent pathogens. However, hrl1 suppresses avirulent pathogen-induced HR cell death. Furthermore, the high PR-1 expression observed in hrl1 remains unaltered after avirulent and virulent pathogen infections. The suppressed HR phenotype in hrl1 is observed even when an elicitor is expressed endogenously from an inducible promoter, suggesting that an impaired transfer of avirulent factors is not the reason. Interestingly, the lack of HR phenotype in hrl1 is reversed if the constitutive defense responses are compromised either by a mutation in NON EXPRESSOR OF PR-1 (NPR1) or by depleting salicylic acid due to the expression of the nahG gene. The rescue of HR cell death in hrl1 npr1 and in hrl1 nahG depends on the extent to which the constitutive systemic acquired response (SAR) is compromised. Pretreating Arabidopsis wild-type plants with SAR-inducers, before pathogen infection resulted in a significant decrease in HR cell death. Together, these results demonstrate that the preexisting SAR may serve as one form of negative feedback loop to regulate HR-associated cell death in hrl1 mutant and in the wild-type plants.Successful host resistance against pathogen invasion requires expeditious recognition and activation of the necessary defense repertoire. One such robust response in plants involves resistance (R) genedependent recognition of pathogen-derived elicitors and initiation of localized cell necrosis at the site of pathogen infection (Goodman and Novacky, 1996). Undoubtedly, the most noticeable feature of this R gene-dependent resistance response is the rapid cell death that is well defined within the attempted infection site, a process known as hypersensitive response (HR). The HR cell death is often preceded by changes in ion fluxes, oxidative burst, and crosslinking of cell wall proteins. Most of the HR cell death processes are accompanied by an increase in salicylic acid (SA) biosynthesis, transcriptional activation of various pathogenesis-related (PR) genes, and the establishment of a long-lasting systemic response known as systemic acquired resistance (SAR; Hammond-Kosack and Jones, 1996;Ryals et al., 1996).Several lines of evidence indicate that HR cell death is a form of programmed cell death that resembles apoptotic cell death in other organisms (Mittler and Lam, 1996; Morel and Dangl, 1997). Identification and analysis of several Arabidopsis mutants with spontaneous cell death that mimic pathogeninduced cell death support the idea that HR cell death may be controlled by plant's own genetic mechanisms (Dangl et al., 1996;Greenberg, 1997;Glazebrook, 1999). Genetic screens aimed at identifying the loss of HR to avirulent pathogens have resulted in the cloning of several R genes. These R genes, when mutated, fail t...